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. 2008 Jun 5;586(Pt 15):3577–3596. doi: 10.1113/jphysiol.2008.152314

Figure 2. Verification of InsP3R-1 dependent channel activity.

Figure 2

A–F, single sweeps from multiple cells following a pulse to −50 mV. A, recording from WT InsP3R-1 in the absence of ADO. B, presence of ADO. C, DT40-3KO cells (InsP3R null cells). D, ADO in the presence of the InsP3R antagonist heparin. E, from a stable DT40-3KO cell line expressing S2+ splice variant D2550A InsP3R-1, a ‘pore-dead’ mutant InsP3R-1. F, from a stable DT40-3KO cell-line expressing S2+ splice variant V2548I InsP3R-1, a mutation in a residue in the putative pore of InsP3R-1 which corresponds to the residue present in ryanodine receptors. G, all-points amplitude histogram; red and blue traces are Gaussian fits of the data. H, I–V relationship for the WT and V2548I InsP3R-1.